This case describes antibody-verified anti-N-methyl-D-aspartate (anti-NMDA) receptor encephalitis in a previously healthy 7 month-old infant female presenting within 48 hours of receiving an influenza booster vaccination during her first influenza season.
A study of the literature on the long-term effects of multiple
immunization over a prolonged period. Except for a small
(approximately 99 persons) follow-up of Fort Detrick personnel,
studies were not directly pertinent to the question. Recommendations
are made for newer screening studies which might be undertaken
on larger groups to resolve this question.
Anti-N-methyl-d-aspartate (Anti-NMDA) receptor encephalitis is an acute autoimmune neurological disorder. The cause of this disease is often unknown, and previous studies revealed that it might be caused by a virus, vaccine or tumor. It occurs more often in females than in males. Several cases were reported to be related to vaccination such as the H1N1 vaccine and tetanus/diphtheria/pertussis and polio vaccines. In this study, we reported an anti-NMDA receptor encephalitis case that may be caused by Japanese encephalitis vaccination. To investigate the association between anti-NMDA receptor encephalitis and vaccination, we analyzed the phylogenetic relationship of the microRNAs, which significantly regulate these vaccine viruses or bacteria, and the phylogenetic relationship of these viruses and bacteria. This reveals that anti-NMDA receptor encephalitis may be caused by Japanese encephalitis vaccination, as well as H1N1 vaccination or tetanus/diphtheria/pertussis and polio vaccinations, from the phylogenetic viewpoint.
Since the implementation of the mass vaccination campaign against hepatitis B in France, the appearance of multiple sclerosis, sometimes occurring in the aftermath of vaccinations, led to the publication of epidemiological international studies. This was also justified by the sharp increase in the annual incidence of multiple sclerosis reported to the French health insurance in the mid-1990s. Almost 20 years later, a retrospective reflection can be sketched from these official data and also from the national pharmacovigilance agency. Statistical data from these latter sources seem to show a significant correlation between the number of hepatitis B vaccinations performed and the declaration to the pharmacovigilance of multiple sclerosis occurring between 1 and 2 years later. The application of the Hill’s criteria to these data indicates that the correlation between hepatitis B vaccine and multiple sclerosis may be causal.
Major media aren’t giving this story the coverage it deserves. I certainly am.
Short question: Can a person sue a US vaccine manufacturer?
Short answer: Under certain conditions, yes.
Note: I’m not framing this article as professional legal advice. I’m reporting what I’ve been able to dig up on a very explosive issue so far. I’ve communicated with two lawyers and a law professor. I’ve been pointed to an important passage on a federal web page.
Right now, lawyers and their clients are suing Merck, the manufacturer, for injuries incurred from Merck’s shingles vaccine, Zostavax.
Among the claimed injuries: contracting shingles; blindness in one eye; partial paralysis; brain damage; death.
I just finished reading a feature article published in The British Medical Journal by BMJ associate editor, Peter Doshi, PhD: “The unofficial vaccine educators: are CDC funded nonprofits sufficiently independent?”
Those who raise concerns about vaccine policy are often asked, “Why aren’t you more balanced?” Perhaps the best response is Doshi’s piece. Is it desirable to seek balance when writing about a topic that is anything but? Faced with the facts, I understand the discomfort.
Vaccination is widely regarded as the greatest medical invention. We are 360° surrounded by vaccine “education.” Children from birth to age 18 receive over 70 doses of 16 vaccines. All of us, from cradle to grave, from newborns, students, and soldiers to pregnant women, healthy adults, health care workers, and the elderly, are exhorted to vaccinate. New programs are constantly being introduced; here’s the latest, the Catch-Up Immunization Scheduler.
In hamster cells transgenic for the DNA of adenovirus type 12 (Ad12) or for the DNA of bacteriophage λ, the patterns of DNA methylation in specific cellular genes or DNA segments remote from the site of transgene insertion were altered. In the present report, a wide scope of cellular DNA segments and genes was analyzed. The technique of methylation-sensitive representational difference analysis (MS-RDA) was based on a subtractive hybridization protocol after selecting against DNA segments that were heavily methylated and hence rarely cleaved by the methylation-sensitive endonuclease HpaII. The MS-RDA protocol led to the isolation of several cellular DNA segments that were indeed more heavily methylated in λ DNA-transgenic hamster cell lines. By applying the suppressive subtractive hybridization technique to cDNA preparations from nontransgenic and Ad12-transformed or λ DNA-transgenic hamster cells, several cellular genes with altered transcription patterns were cloned from Ad12-transformed or λ DNA-transgenic hamster cells. Many of the DNA segments with altered methylation, which were isolated by a newly developed methylation-sensitive amplicon subtraction protocol, and cDNA fragments derived from genes with altered transcription patterns were identified by their nucleotide sequences. In control experiments, no differences in gene expression or DNA methylation patterns were detectable among individual nontransgenic BHK21 cell clones. In one mouse line transgenic for the DNA of bacteriophage λ, hypermethylation was observed in the imprintedIgf2r gene in DNA from heart muscle. Two mouse lines transgenic for an adenovirus promoter-indicator gene construct showed hypomethylation in the interleukin 10 andIgf2r loci. We conclude that the insertion of foreign DNA into an established mammalian genome can lead to alterations in cellular DNA methylation and transcription patterns. It is conceivable that the genes and DNA segments affected by these alterations depend on the site(s) of foreign DNA insertion.
Acellular vaccines against Bordetella pertussis were introduced in Australia in 1997. By 2000, these vaccines had replaced whole-cell vaccines. During 2008–2012, a large outbreak of pertussis occurred. During this period, 30% (96/320) of B. pertussis isolates did not express the vaccine antigen pertactin (prn). Multiple mechanisms of prn inactivation were documented, including IS481 and IS1002 disruptions, a variation within a homopolymeric tract, and deletion of the prn gene. The mechanism of lack of expression of prn in 16 (17%) isolates could not be determined at the sequence level. These findings suggest that B. pertussis not expressing prn arose independently multiple times since 2008, rather than by expansion of a single prn-negative clone. All but 1 isolate had ptxA1, prn2, and ptxP3, the alleles representative of currently circulating strains in Australia. This pattern is consistent with continuing evolution of B. pertussis in response to vaccine selection pressure.